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Angiogenesis is an indispensable mechanism in development and in many pathologies, including cancer, synovitis and aberrant wound healing. Many angiogenic stimulators and inhibitors have been investigated, and some have progressed to the clinic. A disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) is a group of multifunctional proteinases. ADAMTS-1 and ADAMTS-8 have been reported to be anti-angiogenic. Here, we provide evidence that ADAMTS-4, like ADAMTS-1, is expressed by endothelial cells and binds to vascular endothelial groth factor (VEGF). Moreover, ADAMTS-4 inhibited human dermal microvascular endothelial cells (HuDMEC) VEGF-stimulated VEGF receptor (R) R2 phosphorylation, differentiation and migration, suggesting that ADAMTS-4 may be a novel anti-angiogenic molecule.
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http://dx.doi.org/10.1111/j.1365-2613.2011.00802.x | DOI Listing |
Respir Res
March 2025
Department of Respiratory and Critical Care Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, People's Republic of China.
Pulmonary hypertension (PH) is a progressive and life-threatening cardiopulmonary disease that is not uncommon. The modulation of the pulmonary artery (PA) involves various fatty acids, including omega-6 polyunsaturated fatty acids (ω-6 PUFAs) and ω-6 PUFAs-derived oxylipins. These lipid mediators are produced through cyclooxygenase (COX), lipoxygenase (LOX), cytochrome P450 (CYP450), and non-enzymatic pathways.
View Article and Find Full Text PDFCommun Biol
March 2025
Section of Cardiology,, Biological Sciences Division, Department of Medicine, University of Chicago, Chicago, IL, USA.
Myocardial infarction (MI) compromises the cardiac microvascular endothelial barrier, increasing leakage and inflammation. HIF2α, predominantly expressed in cardiac endothelial cells during ischemia, has an unclear role in barrier function during MI. Here, we show that inducible, adult endothelial-specific deletion of Hif2α in mice leads to increased mortality, cardiac leakage, inflammation, reduced heart function, and adverse remodeling after MI.
View Article and Find Full Text PDFCell Death Discov
March 2025
Department of Ophthalmology, Eye & ENT Hospital, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Fudan University, Shanghai, 200031, China.
Fuchs endothelial corneal dystrophy (FECD) is the leading cause of vision-threatening corneal endothelial dystrophy without pharmacologic treatments. Corneal endothelial-mesenchymal transition (cEndMT), a specific cellular phenotypic transition, is implicated in the vicious cycle in FECD pathogenesis. Here, we investigated the reversible epigenetic regulation of N-methyladenosine (mA) during cEndMT process and FECD progression.
View Article and Find Full Text PDFFree Radic Biol Med
March 2025
Department of Pharmacology and Institute of New Drug Development, School of Medicine, Chonbuk National University, Jeonju, Chonbuk, Republic of Korea. Electronic address:
Ann Clin Lab Sci
January 2025
Department of Ophthalmology, TongRen People's Hospital, Tongren, Guihzou, China
Objective: Diabetic retinopathy (DR) is a retinal microangiopathy caused by diabetes mellitus. miRNAs have been shown to be involved in DR-associated micro vessel formation, influence the DR progression, and may be a therapeutic strategy for DR. miRNA-19a-3p is highly expressed in the vitreous of DR patients, however, its mechanism in the occurrence and development of DR is unclear.
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